Methods and apparatus for reducing localized circulatory system pressure

ABSTRACT

The present invention is thus directed to methods and apparatus for decreasing pressure in a first portion of a vessel of the cardiac structure of a patient by implanting a shunt communicating with an area outside said first portion, whereby a volume of blood sufficient to reduce pressure in said first portion is released. Preferably, the first portion comprises the left ventricle and the pressure reduced is the end diastolic pressure, which is accomplished by having the shunt communicate with the left ventricle so a small volume of blood is released from the left ventricle to reduce the end diastolic pressure. Most preferably, the shunt selectively permits flow when a pressure differential between the left ventricle and another chamber of a heart above a threshold pressure, whereby shunting is prevented during left ventricular systole, or, alternatively, selectively permits flow when a pressure differential between the left ventricle and another chamber of a heart is between a lower threshold and a higher threshold, whereby shunting is again prevented during left ventricular systole. In certain embodiments a semi-passive check-valve is controlled and actuated by an external signal, either using a signal generated by an intra-corporeal electrical battery or an externally coupled energy source. In certain embodiments, the shunt has a pump with an input connected to the left ventricle, or other portion with excessive pressure, and an output connected to a volume of lower pressure. The preferred method of implanting the shunt to effect the present invention is by deploying a tubular element having two ends and a tissue affixation element disposed at each of said ends via a catheter, preferably, the fixation element is a shape retaining metallic material that returns to its original shape as part of the retention aspect of its function. In preferred embodiments of the apparatus, the tubular element is comprised of a biologically inert non-metallic material.

[0001] The present invention relates to treatments for reducing specificlocalized points of high pressure within the circulatory system, andmore particularly to methods and apparatus to either acutely orchronically reduce left ventricular diastolic pressure that is createdas a result of congestive heart failure or similar indications.

BACKGROUND OF THE INVENTION

[0002] Congestive heart failure (CHF) is recognized as the most commoncause of hospitalization and mortality in Western society. CHF is anextremely serious affliction that has a great impact on the quality oflife; it involves the loss of heart rate variability and rate responsivemechanisms in the heart, leading to impaired ventricular relaxation andlow exercise tolerance. The disease afflicts about 4 million Americansin any given year; in the USA alone, there are annually about 400,000new cases, 1 million hospital admissions, and $8 billion cost of care.Congestive heart failure is a syndrome characterized by left ventriculardysfunction, reduced exercise tolerance, impaired quality of life anddramatically shortened life expectancy. Decreased contractility of theleft ventricle leads to reduced cardiac output with consequent systemicarterial and venous vasoconstriction. CHF develops generally in thecourse of months or years, and can be the end stage of chronichypertension, infarction, angina, or diabetes. Heart failure, howevercaused, represents an intrinsic property of the muscle, and slowrelaxation due to slow intracellular calcium removal by the sarcoplasmicreticulum is an important factor. In the normal, healthy heart theduration of contraction and relaxation decreases with increasing heartrate. This ensures a diastolic period of sufficient duration, which isimportant (a) for filling of the ventricle, and (b) because coronaryperfusion and myocardial oxygen supply occurs only during diastole. Theduration of contraction and relaxation is determined by calcium removalfrom the contractile filaments, mainly by the calcium pump in thesarcoplasmic reticulum Increased heart rate causes more rapid relaxationdue to increased activation of the calcium pump. The latter mechanism isimpaired in the hypertrophied or failing heart due to reducedtranscription of the genes that supply the calcium pump proteins.Therefore, in heart failure patients an increase of heart rate mayalmost abolish the diastolic interval, which leads to reducedventricular filling, and reduces myocardial blood supply (Davies et al.,1995, “Reduced Contraction and Altered Frequency Response of IsolatedVentricular Myocytes From Patients With Heart Failure,” Circulation 92:2540-2549).

[0003] The syndrome of heart failure is a common course for theprogression of many forms of heart disease. Heart failure may beconsidered to be the condition in which an abnormality of cardiacfunction is responsible for the inability of the heart to pump blood ata rate commensurate with the requirements of the metabolizing tissues,or can do so only at an abnormally elevated filling pressure. There aremany specific disease processes that can lead to heart failure with aresulting difference in pathophysiology of the failing heart, such asthe dilatation of the left ventricular chamber. Etiologies that can leadto this form of failure include idiopathic cardiomyopathy, viralcardiomyopathy, and ischemic cardiomyopathy. The process of ventriculardilatation is generally the result of chronic volume overload orspecific damage to the myocardium In a normal heart that is exposed tolong term increased cardiac output requirements, for example, that of anathlete, there is an adaptive process of ventricular dilation andmyocyte hypertrophy. In this way, the heart fully compensates for theincreased cardiac output requirements. With damage to the myocardium orchronic volume overload, however, there are increased requirements puton the contracting myocardium to such a level that this compensatedstate is never achieved and the heart continues to dilate. The basicproblem with a large dilated left ventricle is that there is asignificant increase in wall tension and/or stress both during diastolicfilling and during systolic contraction. In a normal heart, theadaptation of muscle hypertrophy (thickening) and ventricular dilatationmaintain a fairly constant wall tension for systolic contraction.However, in a failing heart, the ongoing dilatation is greater than thehypertrophy and the result is a rising wall tension requirement forsystolic contraction. This is felt to be an ongoing insult to the musclemyocyte resulting in further muscle damage. The increase in wall stressis also true for diastolic filling. Additionally, because of the lack ofcardiac output, there is generally a rise in ventricular filing pressurefrom several physiologic mechanisms. Moreover, in diastole there is botha diameter increase and a pressure increase over normal, bothcontributing to higher wall stress levels. The increase in diastolicwall stress is felt to be the primary contributor to ongoing dilatationof the chamber.

[0004] Presently available treatments for CHF fall into three generallycategories: (1) pharmacological, e.g., diuretics; (2) assist systems,e.g., pumps; and (3) surgical treatments. With respect topharmacological treatments, diuretics have been used to reduce theworkload of the heart by reducing blood volume and preload. While drugtreatment improves quality of life, it has little effect on survival.Current pharmacological treatment includes a combination of diuretics,vasodilators, inotropes, β-blockers, and Angiotensin-Converting-Enzyme(ACE)-inhibitors (Bristow & Gilbert, 1995, “Improvement in CardiacMyocyte Function by Biological Effects of Medical Therapy: A New Conceptin the Treatment of Heart Failure,” European Heart Journal 16,Supplement F: 20-31). The effect is a decrease of symptoms, and improvedquality of life, but little change in mortality. Moreover, the exercisetolerance of most patients is extremely low, as a consequence of limitedoxygen supply through the lungs. Long lasting lack of exercise andmalnutrition may contribute to the condition and partly explain theexercise intolerance. Indeed, the lack of exercise and deterioration ofcardiac muscle may each contribute to each other, with a snowballingeffect (Coats et al., 1992, “Controlled Trial of Physical Training inChronic Heart Failure: Exercise Performance, Hemodynamics, Ventilation,and Autonomic Function,” Circulation 85: 2119-2131). Clinically, preloadis defined in several ways including left ventricular end diastolicpressure (LVEDP), or left ventricular end diastolic volume (LVEDV).Physiologically, the preferred definition is the length of stretch ofthe sarcomere at end diastole. Diuretics reduce extra cellular fluidthat builds in congestive heart failure patients increasing preloadconditions. Nitrates, arteriolar vasodilators, angiotensin convertingenzyme inhibitors have been used to treat heart failure through thereduction of cardiac workload through the reduction of afterload.Afterload may be defined as the tension or stress required in the wallof the ventricle during ejection. Inotropes such as digoxin are cardiacglycosides and function to increase cardiac output by increasing theforce and speed of cardiac muscle contraction. These drug therapiesoffer some beneficial effects but do not stop the progression of thedisease. Captopril, enalapril and other inhibitors ofangiotensin-converting enzyme (ACE) have been used to treat congestiveheart failure. See Merck Index, 1759 and 3521(11^(th) ed. 1989); Kramer,B. L. et al. Circulation 1983, 67(4):755-763. However, such ACEinhibitors have generally provided only moderate or poor results. Forexample, captopril therapy generally provides only small increases inexercise time and functional capacity. Captopril also has provided onlysmall reductions in mortality rates.

[0005] Assist devices used to treat CHF include, for example, mechanicalpumps. Mechanical pumps reduce the load on the heart by performing allor part of the pumping function normally done by the heart. Currently,mechanical pumps are used to sustain the patient while a donor heart fortransplantation becomes available for the patient. There are also anumber of pacing devices used to treat CHF. However, in the chronicischemic heart, high rate pacing may lead to increased diastolicpressure, indicating calcium overload and damage of the muscle fibers.Finally, there are at least three surgical procedures for treatment ofheart failure: 1) heart transplant; 2) dynamic cardiomyoplasty; and 3)the Batista partial left ventriculectomy. Heart transplantation hasserious limitations including restricted availability of organs andadverse effects of immunosuppressive therapies required following hearttransplantation. Cardiomyoplasty includes wrapping the heart withskeletal muscle and electrically stimulating the muscle to contractsynchronously with the heart in order to help the pumping function ofthe heart. The Batista partial left ventriculectomy includes surgicallyremodeling the left ventricle by removing a segment of the muscularwall. This procedure reduces the diameter of the dilated heart, which inturn reduces the loading of the heart. However, this extremely invasiveprocedure reduces muscle mass of the heart.

[0006] One category of CHF is diastolic heart failure (DHF), whichafflicts between 30% and 70% of those patients with heart failure. DHFis an episodic clinical syndrome that can instigate pulmonary edema,possibly necessitating hospitalization and ventilatory support. Theheart is a complex pump structured of two atria and two ventricles thatpump blood in parallel into the pulmonary circulation at a relativelylow pressure (right ventricle peak systolic pressure is about 25 mmHg)and the systemic circulation (left ventricle peak systolic pressure isabout 120 mmHg). During the diastolic phase of the cardiac cycle theventricles of the heart fill via the respective atria. The pressuredifferential that propels blood from the respective venous circulationsto the atria and ventricles (systemic to the right ventricle andpulmonary to the left ventricle) is low, less than about 5 mmHg. On theleft side, during diastole (when the mitral valve opens), pressure inthe left atrium normally is not more than 12 mmHg. Due to activediastolic relaxation at the onset of diastole, the pressure differencebetween the left atrium and the left ventricle is augmented contributingto the early rapid diastolic filling of the left ventricle. Diastolicpressures in the atrium and the ventricle at this phase of the cardiaccycle drop quickly to less than 5 mmHg and equalize. At this pointduring diastole, the process of filling the left ventricle partiallystops (diastiasis) and is renewed only towards late diastole, whenactive contraction of the atrium occurs, resulting in increased leftatrial pressure and an increased pressure differential between theatrium and the ventricle. Atrial contraction is very important formaintaining adequate left ventricular filling during exercise and otherstates of increased cardiac output demand, or when the left ventriclefails to relax normally such as during ischemia or LV hypertrophy.Toward the end of diastole, pressure in the left ventricle (LVEDP) isincreased but is normally not more than 12 mmHg.

[0007] Disease states in which active and passive relaxation propertiesof the left ventricle are disturbed, or the pumping and emptyingcapacity of the ventricle is reduced, may be translated to increaseddiastolic pressures in the left ventricle. The higher pressures anddistension of the left ventricle cause a rise in wall stress andincreased oxygen consumption. Up to a limit, the increased diastolicpressure and increased ventricular size result in augmented strokevolume. This compensatory mechanism is limited and has a significantphysiologic price mainly when the slope of the pressure-volume curvesturn steep, and left ventricular diastolic pressures becomes markedlyhigh (>20 mmHg). At this point, a state of pulmonary congestion mayensue, turning later to a life threatening state of pulmonary edema.

[0008] A number of cardiovascular diseases can cause significant cardiacdysfunction and lead to the above-mentioned pathophysiologic state andpulmonary edema. These include: hypertension, ischemic heart diseasestate and post myocardial infarction, idiopathic dilated cardiomyopathy,valvular heart disease, including aortic stenosis, mitral stenosis,aortic regurgitation, mitral regurgitation, and combined valvular heartdisease. Other primary myocardial diseases such as post partum andhypertrophic cardiomyopathy may cause similar conditions. In all thesedisease states with either decreased ability for the left ventricle topump blood (systolic dysfunction) or reduced fling capacity (diastolicdysfunction) left ventricular diastolic pressure rises. Increaseddiastolic pressure in the left ventricle eventually in and of itselfbecomes a cause for greater degradation in cardiac function thanoccurred as a result of the original insult. The augmented pressures maycause as stated previously pulmonary congestion and dyspnea. At extremeconditions the clinical state may deteriorate to pulmonary edema.

[0009] There are several known techniques to attempt to overcome thestate of left ventricular dysfunction, increased diastolic leftventricular pressures and pulmonary congestion. However, none are fullysatisfactory. For example, pharmacological treatments are the onlypractical methods for chronic therapy for most of the population withcongestive heart failure. The pharmacological agents used to treatcongestive heat failure result in a reduction in diastolic pressure andprevention of pulmonary and peripheral congestion discussed above, i.e.,diuretics, vasodilators and digoxin. Diuretics reduce the volume loadand thereby reduce preload and diastolic wall stress. Vasodilators havea dual effect in reducing arterial resistance as well as increasingvenous capacitance, thereby reducing preload and after load and wallstress throughout the cardiac cycle. These drugs, either direct actingon the vasculature or via neurohormonal mechanisms (ACE inhibitors), arelimited in their effect since they may cause hypotension in asignificant number of patients with myocardial dysfunction. Thesepharmacological agents are of limited value mainly because of their sideeffects. The use of diuretics is associated with side effects related tothe drugs and to the detrimental effect on renal function. Vasodilatorshave also many side effects some of which limit the use of the drugs andtheir efficacy including hypotension in many patients. Drug therapyresults in many of the patients in relative clinical stability. However,episodes where intraventricular diastolic pressure may rise abovephysiologic needs for cardiac stroke volume augmentation and culminateinto pulmonary edema occur often and are very difficult to manage.

[0010] In extreme acute situations, temporary assist devices andintraaortic balloons may be helpful. Cardiac transplantation and chronicLVAD implants are solutions available for a small part of the patientpopulation and as last resort. However, all the assist devices currentlyused are intended to improve pumping capacity of the heart and increasecardiac output to levels compatible with normal life. Finally, cardiactransplantation is another solution, but is not a very practical and islimited to extreme cases and as are the various assist devices. Themechanical devices were built to allow propulsion of significant amountof blood (liters/min) and this is also their main technologicallimitation. The need for power supply, relatively large pumps and dangerof hemolysis and infection are all of significant concern.

[0011] Thus, there exists a long-felt and as of yet unsolved need for atreatment that addresses the course of congestive heart failure, and inparticular the high pressure of the left ventricle and the compoundingfactors that are associated with it. It would therefore be desirable toprovide methods, apparatus and treatments that beneficially reduce andregulate the pressure within the left ventricle. It is an object of thepresent invention to provide methods and apparatus for reducing leftventricular end diastolic pressure, and more particularly to providemethods and apparatus without deleterious side effects. It is a furtherobject of the present invention to provide methods and apparatus thatcan be used in a minimally invasive manner for both acute and chronictreatments.

SUMMARY OF THE INVENTION

[0012] The present invention reduces the increased diastolic pressurethat can occur as part of the clinical syndrome referred to asCongestive Heart Failure (CHF). Passive and semi-passive devices toreduce left ventricular end-diastolic pressure are disclosed, and inpreferred embodiments, a shunt-type device allows a small volume ofblood to be released from the left ventricle to reduce the pressure.Certain embodiments use a passive check-valve that allows flow onlyabove a given threshold pressure, while others use a passive check-valvethat allows flow only within a window between a lower pressure thresholdand a higher-pressure threshold. Embodiments employing check valvesprevent shunting during left ventricular systole. Alternatively,semi-passive embodiments have a valve activated by and external signal,such as an intra-corporeal electrical battery or an externally coupledenergy source. A third type of preferred embodiment of the inventionemploys an device such as a pump to actively move blood, with the intentof preventing further deterioration of the patient's heart failure orallowing for some reversal of the heart failure. For example in patientspresenting with diastolic heart failure (DHF) the present inventionprevents this occurrence by reducing diastolic pressures in the leftatrium below the excessive levels that would otherwise have causedpulmonary edema.

[0013] The present invention is thus directed to methods and apparatusfor decreasing pressure in a first portion of a vessel of the cardiacstructure of a patient by implanting a shunt communicating with an areaoutside said first portion, whereby a volume of blood sufficient toreduce pressure in said first portion is released. Preferably, the firstportion comprises the left ventricle and the pressure reduced is the enddiastolic pressure, which is accomplished by having the shuntcommunicate with the left ventricle so a small volume of blood isreleased from the left ventricle to reduce the end diastolic pressure.Most preferably, the shunt selectively permits flow when a pressuredifferential between the left ventricle and another chamber of a heartabove a threshold pressure, whereby shunting is prevented during leftventricular systole, or, alternatively, selectively permits flow when apressure differential between the left ventricle and another chamber ofa heart is between a lower threshold and a higher threshold, wherebyshunting is again prevented during left ventricular systole. In certainembodiments a semi-passive check-valve is controlled and actuated by anexternal signal, either using a signal generated by an intra-corporealelectrical battery or an externally coupled energy source. In certainembodiments, the shunt has a pump with an input connected to the leftventricle, or other portion with excessive pressure, and an outputconnected to a volume of lower pressure. The preferred method ofimplanting the shunt to effect the present invention is by deploying atubular element having two ends and a tissue affixation element disposedat each of said ends via a catheter, preferably, the fixation element isa shape retaining metallic material that returns to its original shapeas part of the retention aspect of its function. In preferredembodiments of the apparatus, the tubular element is comprised of abiologically inert non-metallic material.

BRIEF DESCRIPTION OF THE DRAWINGS

[0014]FIG. 1 is a perspective view of a first embodiment of animplantable shunt made in accordance with the present invention;

[0015]FIG. 2 is a side elevation view, in cross-section as shon by lines2-2 in FIG. 1, illustrating the placement of the shunt shown in FIG. 1in a septum, and showing diagrammatically the use of a pump to augmentflow in certain embodiments; and

[0016] FIGS. 3-5 are a cross sectional view of a patient receiving ashunt made in accordance with the present invention via percutaneousplacement.

DETAILED DESCRIPTION OF THE PREFERRED EMBODIMENTS

[0017] Referring now to FIG. 1, there is shown a perspective view of afirst embodiment of a shunt 100 made in accordance with the presentinvention. The shunt 100 is comprised of a fixation element 110, whichis shown as a planar circular element. It will be understood, however,that the fixation element 110 can be circular, polygonal, spiral or manyother shapes. Moreover, the fixation element can lie in a single planeor be curved in multiple planes, such as in a helical configuration. Itcan be constructed of a variety of materials that offer the elasticrange and spring-like characteristics that will enable passage through acatheter lumen, or through the lumen of another implantation assistancedevice, in a relatively straightened configuration and then recovery ofits fill fixation configuration shape. In certain embodiments, thefixation element can be made of reduced size and then expanded throughthe use of shape-memory alloys (SMA's), such as nickel-titanium (NiTi,also known as nitinol), that change shape in response to temperaturechanges and which are fabricated such that the temperature change frombelow body temperature to body temperature causes the shape conversionnecessary for implantation. If SMA materials are not used, suitablematerials include super-elastic metals, such as NiTi or stainless steel,such as the alloy Elgiloy, commonly used for medical implants.Additionally, polymeric materials can be used to form the fixationelement or as a coating over a metallic core. The fixation element maybe coated and/or textured as so as to increase its biocompatability orto increase the degree to which it quickly becomes endothelialized,which may be desired in some implantation conditions.

[0018] As illustrated, the fixation element 110 surrounds and positionsthe shunt tube element 120, which is provided so as to enable passage ofblood from a region of high pressure, such as the left atrium, to aregion of lower pressure, such as the right atrium. The dimensions ofthe shunt tube element 120 are chosen so as to be as small as possiblewhile still allowing sufficiently rapid fluid flow without endangeringblood coagulation induced by blood stasis or low-flow zones.Computational fluid dynamics methods can be used to appropriately shapethe element so as to minimize low-flow zones and maximize laminar flow.The inside diameter of the shunt tube is preferably greater than 1 mmand less than 5 mm, but it will be understood that a wide range ofshapes and diameters can be constructed that will effect the purpose ofthe present invention in a variety of patients and flow conditionswithin those patients. The shunt tube element 120 is preferably formedof either metallic or polymeric materials and may be coated and/ortextured as mentioned above. Pyrolitic carbon coating, as is commonlyused in implantable mechanical heart valves, can be used to increase thedegree to which the surface is biologically inert. Examples of suchcommercially available materials include On-X{circle over (R)} Carbon,from Medical Carbon Research Institute, LLC, of Austin, Tex.

[0019] Also illustrated in FIG. 1 is a valve element 130, which asexplained below is not necessarily included in all embodiments withinthe scope of the present invention and can be of a variety of forms. Asillustrated a leaflet 131,132 can be used, either in a single piece oras a dual leaflet design as illustrated. In the embodiment shown in FIG.1, each leaflet 131,132 is a flat plate that pivots to open and closethe orifice of the shunt tube. A ball-and-socket design can be used aswell. Another alternative design is the duckbill-type valve. The valveelement can be formed using the same range or materials and coatingsmentioned above for the shunt tube.

[0020] From the foregoing, it will be appreciated by those of skill inthe art that the present invention is well adapted to percutaneousplacement via femoral access, however, other implantation techniquessuch as surgical techniques using either an open chest procedure orthose using minimally invasive techniques are also within the scope ofthe present invention.

[0021] The concepts of allowing pressure to be relieved in one area ofthe circulation by shunting to an area of lower pressure as disclosedherein may take many embodiments, all of which will be apparent to thoseof skill in the art upon review of the foregoing descriptions of thephysiology and medicine involved, and the description of the embodimentof FIG. 1.

[0022] In accordance with the present invention, the device may or maynot include the valve element 130, since in certain patients or to treatcertain conditions a valve would add complexity while not providingnecessary functionality. Similarly, depending upon the circumstances ofuse, the valve element 130 may be either passive (actuated by the forceof blood) or active (actuated by some other portion of the device). Inactive valve embodiments, the valve element 130 may include electric orelectromagnetic elements that can be selectively actuated to open andclose the valve element 130 or, if the valve element is designed forgradual opening and closing, move the valve element 130 between a firstpositions and a second position. In some embodiments, the valve will bechosen and designed so that it responds only upon certain conditionsoccurring within the heart, such as the following: absolute left atrialpressure, differential atrial pressure, other intra-cardiac pressures,other cardiovascular pressures, or other physiological conditions thatmight correlate to an exacerbated state of diastolic heart failure, suchas blood oxygen saturation or pH. In such embodiments, response to anygiven pressure or differential pressure will imply that a portion of theimplanted device is in fluid communication with the relevant pressuresource or sources. These embodiments will provide robust and reliablefunctionality by being mechanical and operating with signal inputs. Allshunts, whether they include a valve or not can be further enhanced byincluding a check-valve that will prevent backflow. Those of skill inthe art will appreciate that it is typically desirable to prevent flowfrom the right heart to the left heart, and thus one or more checkvalves can be appropriately placed. A double-check valve allows bloodpressure above a lower limit but below a higher limit to actuate thevalve, thus in a preferred embodiment, shunting blood from the left sideto the right side only during a period of diastole.

[0023] Referring now to FIG. 2, another aspect of the devices of thepresent invention is that the shunt 100 may or may not be in fluidcommunication with a pump 140, such as either a surgically implantedpump that continuously moves a small amount of blood from one chamber orarea to another, for example from the left ventricle chamber to theaorta for chronic reduction of LVEDP. Alternatively, the invention caninclude a catheter-based pump that continuously moves a small amount ofblood from the LV chamber to the aorta for acute reduction of LVEDP. Incertain preferred embodiments, the pump and valve will have aheart-synchronized actuated valve to allow specific regimens ofleft-to-right shunting to be applied. As seen in FIG. 2, after the shunt100 is placed in a septum or other area, the pump 140 may be placed soas to direct fluid toward the shunt, the pump may be directly connectedto the shunt, juxtaposed to the shunt, or displaced from the shunt butcapable of directing flow in such a way as to effect more efficientpressure reduction.

[0024]FIG. 2 shows an implant similar to that of FIG. 1 that is placedsurgically for the chronic reduction of LVEDP. This device includes arelatively small-sized pump, which can be similar to those used inLeft-Ventricular Assist Devices (LVADs). Unlike the LVAD, however, thedisclosed invention does not seek to significantly “support” thefunction of the left ventricle by pumping blood from the LV chamber tothe body. Rather, it is intended only to “offload” the excessivepressure that builds through the diastolic phase of the cardiac cycle insome CBF patients. Whereas a normal LVEDP is in the range of 6-12 mmHg,patients with diastolic dysfunction heart failure (DDHF), end-diastolicpressure (EDP) in the left atrium (LA) and left ventricle (LV) can riseconsiderably above normal levels. Therefore the present inventionencompasses a number of embodiments that are both capable of beingeither implanted during a surgical procedure or using a catheter(percutaneous). The shunt 100 allows blood to flow in the directionshown by the arrows so long as there is a lower pressure in the chamberor vessel adjoining the LV. In any embodiment, the methods and apparatusof the present invention reduce EDP, and in particular mitigate the mostsevere consequences of significantly increased EDP, such as pulmonaryedema.

[0025] Thus, in preferred embodiments of the present invention the shuntis disposed in a wall between the chambers of a patient's heart, andmost preferably, disposed in the atrial septum to permit blood to flowfrom the left ventricle when the pressure within the ventricle exceedsthe pressure of the adjoining atrial chamber. In another particularembodiment, a sophisticated shunt apparatus implanted in theintra-atrial septum to allow intermittent and controlled blood flow fromthe left atrium to the right atrium (RA), thereby reducing LAEDP.Alternatively, the shunt might have its origin in locations other thanthe LA, such as the LV, and might have its output at locations otherthan the RA, such as the light ventricle (RV).

[0026] As explained above, although one class of embodiments of thepresent invention is designed to be purely mechanical and will havecertain advantages, the present invention also encompasses additionalembodiments wherein additional features such as internal signalprocessing and an energy source, such as a battery, are included. Insuch embodiments, the shunts described above will include a valveapparatus that responds to conditions other than those occurring withinthe heart and/or has internal signal processing requiring an energysource. A device of this type responds according to programmedalgorithms to all of the conditions mentioned above. The signalprocessing ability of devices in such embodiments enable adaptiveapproaches as well, in which the device response to conditions willchange over time according to a pre-programmed adaptation algorithm.Such embodiments will include additional apparatus, such as a powersource, sensors and the like. The provision of implantable, programmableelectrical devices that collect cardiac data and effect the operation ofcertain other elements of a device are well known in the field ofcardiac pacing, for one example. In one particular embodiment, theactively controlled valve of the shunt as in senses and responds toelectrical signals so as to act in synchronization with the cardiaccycle.

[0027] Either passive or active devices may be linked to an externalindicator, such as pendant worn by the patient, that displays the devicestatus. Such an indicator enables the patient to notify a physician inthe event of an activation of the implanted device that corresponds tothe significantly exacerbated state heart failure. In this case, thedevice will be acting to prevent the occurrence of pulmonary edemaduring the time that the patient notifies a physician and then undergoesmedical treatment to reduce the severity of the patient's condition.

[0028] Similarly, any embodiment of the present invention may bedesigned so that an external device can be used on occasion to eithermechanically adjust (in the case of passive devices; for example, bymagnetic coupling) and/or to reprogram (in the case of active devices)the functioning of the implanted device.

[0029] The methods mentioned above will prevent from excessive pressuresto build up in the left ventricle and help restore wall stress indiastole and systole to normal values quickly thus helping theintroduction of pharmacological agents as adjunct therapy or vice versa.This mode of therapy will be complementary to the current management ofthe patients and allow more controlled stabilization. It can be added asa component of cardiac pacemaker (dual or biventricular) and derive thepower supply from the pacemaker battery.

[0030] The pressure/flow/volume requirements of the various embodimentsof the present invention will be determined using methodologies similarto those used to design a Left Ventricular Assist Device (LVAD) but withcertain distinctly different flow requirements, rather than the intentof supporting systemic circulation requirements found in a LVAD. Thus,certain shunts made in accordance with the present invention can usedesigns and dimensions that would not be appropriate or adequate for anLVAD. Patients with hear failure dominated by systolic dysfunctionexhibit contraction abnormalities, whereas those in diastolicdysfunction exhibit relaxation abnormalities. In most patients there isa mixed pathophysiology. Normal pulmonary venous pressure (PVP)necessary for the normal LV to adequately fill and pump is less than 12mmHg. Patients with systolic dysfunction have larger LV volume tomaintain SV and may need increased PVP to fill (mixed systolic diastolicdysfunction). Patients with diastolic dysfunction need increased PVP forthe LV to fill and adequately pump.

[0031] The hemodynamic performance of the present invention, and thusthe design of the shunt and its actuation, placement etc. will bedetermined by a variety of factors, for example, the following table isin the form of:

[0032] IF ({LAEDP} AND/OR {Mean LA P}) AND/OR ({□ LAEDP−RAEDP} AND/OR {□Mean LA P−Mean RA P}) THEN {ACTION}

[0033] In which LAEDP, Mean LA P, RAEDP and Mean RA P refer to minima,maxima or ranges for the respective pressures (please specify which inthe table), and the AND/OR indicate that a logical operator or an NA(not applicable) should be entered S     A □ Then c N (Action) e D M n ea / a r n i O o R a t r i a l P E N N Remove sufficient blood from x A Athe LA to reduce LA pressure by 5 mmHg

[0034] Thus for example, a chronic device can be a preventive devicewhere when pressures rise for some reason to dangerous levels the pumpgoes into action and helps to lower the pressure in the left ventricle,thereby preventing the acute development of dyspnea and pulmonary edemaand assures that the LVDP are always at an optimal level of no more than15 mmHg.

[0035] In other embodiments and for other indications, the presentinvention might move an extra volume of blood from the LV into theaorta. To do so, the pump 140 must be capable of moving blood from achamber exhibiting 20 mmHg in diastole to 70 mmHg in the aorta. Anotherpossible chamber where blood from the LA (throughout the cardiac cycle)or LV (only in diastole) can be directed to is the Right Atrium, andalternatively right ventricle. The benefit of directing blood from LA toRA is that the pressure differences are smaller and the blood can bemoved in diastole and systole as well. Filling of the atria (R and L)during the systolic phase of the cardiac cycle determines the pressurein the atria at the onset of diastole and the opening of the valves.

[0036] Those of skill in the art will appreciate that there are a numberof techniques for placement and locations for placement of shunts madein accordance with the present invention. For example, a surgicallyimplanted passive shunt can be placed between the left ventricle and theright atrium for chronic reduction of LVEDP. Alternatively, a surgicallyimplanted passive shunt can be placed between the left atrium and theright atrium for chronic reduction of LVEDP. For percutaneous placement,a catheter-based passive shunt can be inserted from the right atriumtrans-septally into the left atrium for acute reduction of LVEDP.Another catheter-delivered embodiment is a passive shunt that isimplanted from the right atrium trans-septally into the left atrium forchronic reduction of LVEDP.

[0037] Although the present invention provides new and useful methods oftreatment, the techniques of implanting shunts as described herein iswell known. For one example, in a preferred embodiment of the presentinvention, as illustrated in FIGS. 3-5, a transseptal needle set isadvanced toward the wall of the right atrial septum. Access has beenmade from the femoral vein with the system being advanced through theinferior vena cava and into the right atrium. Devices that allow suchaccess and subsequent transseptal puncture are available from CookIncorporated. For example, the procedure can be carried out using astainless steel and obrturator set TSNC-18-71.0 for adults andTSNC-19-56.0 for pediatric patients. Once transseptal puncture has beenachieved, a guidewire is exchanged for the needle component in thecommercially available device described above and then passed into theleft atrium. The process of securing catheter access to the left atriumby way of a transseptal puncture is further described in the standardmedical text Braunwald, Heart Disease, (Ch. 6, p. 186) which isincorporated herein by reference. After the transseptal sheath ispositioned in the left atrium, as describe above, the placement of ashunt made in accordance with the present invention is initiated. Thefollowing is a generalized sequence; the placement procedure will bedone according to the typical methods of interventional cardiology asare well known to physicians trained in that subspecialty. The typicalsupporting apparatus found in the cardiac catheterization laboratorywill be used, such as fluoroscopy for visualization and hemodynamic andECG monitoring equipment to assess catheter position and patient vitalsigns.

[0038] The dilator and wire will be withdrawn from the sheath that nowextends from the femoral vein access point in the patient's groin to theleft atrium, traversing the femoral vein, the illiac vein, the inferiorvena cava, the right atrium, and the atrial septum The delivery catheterwill be passed through the sheath while under fluoroscopicvisualization. Radiopaque markers are provided on this catheter as wellas the sheath in order to locate specific points. The delivery catheteris carefully and slowly advanced so that the most distal portion of theleft-atrial fixation wire is emitted from the distal opening of thecatheter and into the chamber of the left atrium. The fixation wire isformed from a spring-like material and/or may be super-elastic ofshape-memory alloy, so that as it leaves the constraint provided by theinner lumen of the delivery catheter, it reforms into its fully formedshape, which may circular or polygonal as previously disclosed. Theassembly of the sheath and the delivery catheter are then slowlyretracted en bloc so as to withdraw the fixation wire towards the atrialseptum. The physician stops this retraction when it becomes apparent byfluoroscopic visualization as well as by tactile feedback that thefixation wire has become seated against the atrial septum. At thatpoint, the sheath alone is retracted, uncovering the shunt andpositioning it within the opening that has been created within theatrial septum. The sheath is then further retracted, allowing theright-atrial fixation wire to reform into its fully formed shape. Theentire shunt assembly is then detached from the delivery catheter systemThe shunt is controlled within the delivery catheter by means of longcontroller wire that has independent translational control within thecatheter lumen. This attachment is formed by any conventional method,e.g., a solder or adhesive or the like that will mechanically detach ata prescribed tension level, that level being exceeded by the physicianat this point in the procedure by firmly retracting the controller wire.

[0039] Although certain embodiments have been set forth and describedherein, numerous alterations, modifications, and adaptations of theconcepts presented will be immediately apparent to those of skill in theart, and accordingly will lie within the scope of the present invention,as defined by the claims appended hereto.

What is claimed is:
 1. Apparatus for decreasing pressure in a firstportion of a vessel of the cardiac structure of a patient comprising ashunt communicating with an area outside said first portion, whereby avolume of blood sufficient to reduce pressure in said first portion isreleased.
 2. The apparatus of claim 1, wherein the first portioncomprises the left ventricle and said pressure is the end diastolicpressure in a patient heart, wherein said shunt communicates with theleft ventricle, whereby a small volume of blood is released from theleft ventricle to reduce the end diastolic pressure.
 3. The apparatus ofclaim 2, wherein the shunt comprises a passive check-valve that allowsflow when a pressure differential between the left ventricle and anotherchamber of a heart above a threshold pressure, whereby shunting isprevented during left ventricular systole
 4. The apparatus of claim 2,wherein the shunt comprises a passive check-valve that allows flow whena pressure differential between the left ventricle and another chamberof a heart is between a lower threshold and a higher threshold, wherebyshunting is prevented during left ventricular systole
 5. The apparatusof claim 2, wherein the shunt comprises a semi-passive check-valvecomprising a valve activated by an external signal.
 6. The apparatus ofclaim 5, wherein an intra-corporeal electrical battery generates saidsignal.
 7. The apparatus of claim 5, wherein signal is generated by anexternally coupled energy source.
 8. The apparatus of claim 2, furthercomprising a pump in fluid communication with the shunt and having aninput connected to the left ventricle and an output connected to avolume of lower pressure.
 9. The apparatus of claim 2, comprising atubular element having two ends and a tissue affixation element disposedat each of said ends.
 10. The apparatus of claim 8, wherein said tubularelement is comprised of a biologically inert non-metallic material. 11.A method of decreasing pressure in a first portion of a vessel of thecardiac structure of a patient comprising the step of implanting a shuntcommunicating with an area outside said first portion, whereby a volumeof blood sufficient to reduce pressure in said first portion isreleased.
 12. The method of claim 11, wherein the first portioncomprises the left ventricle and said pressure is the end diastolicpressure in a patient heart, wherein said shunt communicates with theleft ventricle, whereby a small volume of blood is released from theleft ventricle to reduce the end diastolic pressure.
 13. The method ofclaim 12, further comprising the step of selectively permitting flowwhen a pressure differential between the left ventricle and anotherchamber of a heart above a threshold pressure, whereby shunting isprevented during left ventricular systole
 14. The method of claim 12,further comprising the step of selectively permitting flow when apressure differential between the left ventricle and another chamber ofa heart is between a lower threshold and a higher threshold, wherebyshunting is prevented during left ventricular systole
 15. The method ofclaim 12, further comprising the step of actuating a semi-passivecheck-valve by an external signal.
 16. The method of claim 15, furthercomprising the step of generating said signal with an intra-corporealelectrical battery.
 17. The method of claim 15, further comprising thestep of generating said signal with an externally coupled energy source.18. The method of claim 12, further comprising the step of activating apump in fluid communication with the shunt and having an input connectedto the left ventricle and an output connected to a volume of lowerpressure.
 19. The method of claim 12, further comprising the step ofimplanting said shunt, said implanting step comprising the step ofdeploying a tubular element having two ends and a tissue affixationelement disposed at each of said ends via a catheter.
 20. The method ofclaim 19, wherein said tissue fixation element is a shape retainingmetallic material and further comprising the step of releasing thetissue fixation elements.